We report a 22 year old male who was admitted to our hospital with alleged
history of consumption of monocrotophos poison and had presented with chest
pain. His electrocardiogram (ECG) had showed ST segment elevation myocardial
infarction and troponins were elevated. He also had low cholinesterase levels and
was treated with pralidoxime and atropine and his condition improved. Cardiac
catheterization showed patent coronaries. Acute coronary syndrome is a rare
manifestation of organophosphorus compound (OPC) poisoning. The current case
and subsequent review of literature tells us the need for close cardiac monitoring
of all patients with OPC poisoning.

Introduction

OPC poisoning is very common
in India where farmers form a
significant proportion of the population
who commonly use it as insecticides.
OPC poisoning can cause cholinergic
symptoms like salivation, lacrimation,
urination and defecation. Nicotinic
symptoms like neck muscle weakness,
ocular weakness, proximal muscle
weakness and respiratory muscle
weakness can occur as a part of
intermediate syndrome. ECG changes like transient ST-T wave changes, QT
prolongation, atrial and ventricular
arrhythmias can occur1. Few cases
of myocardial infarction (MI) after
OPC poisoning has been reported. We
report a young man who developed
myocardial infarction after OPC
(monocrotophos) poisoning.

Case

22 year old young man got admitted
in our toxicology ward with alleged
history of consumption of 15 ml of monocrotophos poison in his house.
He was initially taken to the nearby
private hospital where gastric lavage
and activated charcoal was given. He
had presented to the hospital with
complaints of chest pain. Chest pain
was left sided and diffuse and 8/10
in intensity. He also had shortness of
breath at the time of presentation. No
palpitation or syncope was noted. He
also had increased salivation. Review
of system was negative for other
complaints. He had no significant past
medical history. He was a nonsmoker
and did not drink alcohol. He was not
allergic to any medications. Physical
examination revealed moderately built
male. Cardiopulmonary examination
was clinically normal. Abdomen was
soft and he had bilateral constricted
pupils on neurological examination.
ECG which was taken revealed ST
elevation in leads II, III, AVF (Figure-
1).His vitals were stable. He was
then referred to the government
general hospital, Chennai. In our
center, serum CPK-MB, troponins
were immediately done which were
elevated. Echocardiogram was done
which showed regional wall motion
abnormality in the inferior wall of the
left ventricle. Serum cholinesterase
levels were 1172 IU/dl which is
low. Serum homocysteine levels,
PT/INR, APTT, antithrombin, lupus
anticoagulant and anticardiolipin
antibodies were within normal limits.
On the next day serum pro-NT BNP
levels was done which was elevated.
Patient was treated with pralidoxime,
atropine, anticoagulant and antiplatelet
drugs. Following this treatment, the
patient’s serum cholinesterase levels
improved, chest pain recovered.
Coronary angiogram (Figure 2) was
done the next day which was found to
be normal. Patient’s medical condition
improved and he was discharged.

Discussion

Cardiac complications often
accompany poisoning with OPC. These
may be serious and often fatal, being
represented by cardiac arrhythmias,
electrocardiographic abnormalities
and conduction defects, as well as
MI, a rarely reported complication
of OPC poisoning. The extent and
pathogenesis of cardiac toxicity from
these compounds is not yet clearly
defined. In literature we had few cases
of MI occurring after OPC poisoning.
Lionte C et al1 reported a 57 year old woman who developed anteroseptal MI
and succumbed to death. Kiss Z et al2
reviewed 168 cases of OPC poisonings
with special respect to frequent
arrhythmias. In five patients a transient
picture of MI was seen. Dayton S.B et
al3 reported increased risk of MI among
farm women exposed to pesticides.
A rare case of MI due to parathion
poisoning was reported by Yajneesh
kidiyoor et al.4 The affected patient
was a farmer from rural India who
had succumbed to the complications
of MI. Madhu Pankaj5 et al reported
a 30 year old male who had taken
chlorpyrifos and had presented with
anterior wall myocardial infarction.
Edibe Karasu6 et al also reported a 52
year old patient who had presented
with inferior wall myocardial infarction
after parathion ingestion. In patients
with angiographically smooth coronary
arteries, acetylcholine has been
reported to produce both vasodilation
and constriction. The development
of vasoconstriction is likely to be an
abnormality of endothelial function
that precedes atherosclerosis or an
early marker of atherosclerosis not
detectable by angiography. This is
a likely mechanism in our patient.Coronary vasoconstriction response
in isolated perfused heart mediated
by M 3 receptor has been reported in
rats. The cardiovascular manifestations
also reflect mixed effects on the
autonomic nervous system. Increased
sympathetic tone is often initially
present and most patients manifest
as sinus tachycardia and sometimes
hypertension. As toxicity becomes more
severe, bradycardia with a prolonged
PR interval and atrio-ventricular blocks of various degrees occur because of
excessive parasympathetic tone and
possibly because of reduced coronary
blood flow.

Conclusion

Cardiac complications often
accompany poisoning with OPC,
particularly during the first few
hours. Hypoxemia, acidosis, and
electrolyte derangements are major
predisposing factors. Close monitoring
in intensive or coronary care facilities
with administration of antidotes in
adequate doses early in the course of
the illness will improve the outcome.

Conflict of interest

The authors of the paper declare that
there is no conflict of interests involved
regarding the publication of this paper.

Acknowledgement

We thank all the faculty of Institute
of Internal Medicine, Madras Medical
College for their kind help rendered in
the evaluation of this case report.